Distinct Electrogram Features and Ventricular Arrhythmia Induction Modes Between Repolarization and Conduction Heterogeneities.

J wave syndromes electrogram fragmentation idiopathic ventricular fibrillation sudden cardiac death ventricular fibrillation

Journal

JACC. Clinical electrophysiology
ISSN: 2405-5018
Titre abrégé: JACC Clin Electrophysiol
Pays: United States
ID NLM: 101656995

Informations de publication

Date de publication:
04 Apr 2024
Historique:
received: 04 10 2023
revised: 01 03 2024
accepted: 04 03 2024
medline: 25 4 2024
pubmed: 25 4 2024
entrez: 25 4 2024
Statut: aheadofprint

Résumé

Recent clinical studies have indicated the presence of localized electrical abnormalities in idiopathic ventricular fibrillation and J-wave syndrome patients. This study aims to characterize the specific electrical signatures of localized repolarization and conduction heterogeneities and their respective role in vulnerability to arrhythmias. Optical mapping was performed in porcine right ventricles with local: 1) repolarization shortening; 2) conduction slowing; or 3) structural heterogeneity induced by locally perfusing: 1) pinacidil (20 μmol/L, n = 13); or 2) flecainide (2 μmol/L, n = 13) via an epicardial catheter; or 3) by local epicardial tissue destruction (9 radiofrequency lesions n = 12). Electrograms were recorded (n = 5 in each group) and spontaneous and induced arrhythmias were quantified and optically mapped. Electrograms were normal in (1) but showed local fragmentation in 40% of preparations in (2) with greater effects observed at high pacing frequencies dependent on the wavefront direction. In (3), the structural substrate alone increased the width and number of peaks in the electrograms, and addition of flecainide induced pronounced fragmentation (≥3 peaks and ≥70 ms) in all cases. Occurrence of spontaneous arrhythmias was significantly increased in (1) and (2) (P < 0.0001 and 0.05, respectively, vs baseline) and were triggered by ectopies. Vulnerability to arrhythmias at high pacing frequencies (≥2 Hz) was the lowest in (1) and greatest in (2). Microstructural substrates have the most pronounced impact on electrograms, especially when combined with sodium channel blockers, whereas local action potential duration shortening does not lead to electrogram fragmentation even though it is associated with the highest prevalence of spontaneous arrhythmias.

Sections du résumé

BACKGROUND BACKGROUND
Recent clinical studies have indicated the presence of localized electrical abnormalities in idiopathic ventricular fibrillation and J-wave syndrome patients.
OBJECTIVES OBJECTIVE
This study aims to characterize the specific electrical signatures of localized repolarization and conduction heterogeneities and their respective role in vulnerability to arrhythmias.
METHODS METHODS
Optical mapping was performed in porcine right ventricles with local: 1) repolarization shortening; 2) conduction slowing; or 3) structural heterogeneity induced by locally perfusing: 1) pinacidil (20 μmol/L, n = 13); or 2) flecainide (2 μmol/L, n = 13) via an epicardial catheter; or 3) by local epicardial tissue destruction (9 radiofrequency lesions n = 12). Electrograms were recorded (n = 5 in each group) and spontaneous and induced arrhythmias were quantified and optically mapped.
RESULTS RESULTS
Electrograms were normal in (1) but showed local fragmentation in 40% of preparations in (2) with greater effects observed at high pacing frequencies dependent on the wavefront direction. In (3), the structural substrate alone increased the width and number of peaks in the electrograms, and addition of flecainide induced pronounced fragmentation (≥3 peaks and ≥70 ms) in all cases. Occurrence of spontaneous arrhythmias was significantly increased in (1) and (2) (P < 0.0001 and 0.05, respectively, vs baseline) and were triggered by ectopies. Vulnerability to arrhythmias at high pacing frequencies (≥2 Hz) was the lowest in (1) and greatest in (2).
CONCLUSIONS CONCLUSIONS
Microstructural substrates have the most pronounced impact on electrograms, especially when combined with sodium channel blockers, whereas local action potential duration shortening does not lead to electrogram fragmentation even though it is associated with the highest prevalence of spontaneous arrhythmias.

Identifiants

pubmed: 38661605
pii: S2405-500X(24)00180-4
doi: 10.1016/j.jacep.2024.03.002
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures This study received financial support from the French Government as part of the “Investments of the Future” program managed by the National Research Agency (ANR-10-IAHU04-LIRYC). It was funded by the Leducq-Foundation (RHYTHM network, 16CVD02), the Fondation Coeur et Artères (FC17T2), and the European Research Council (ERC-2021-ADG 101054717). All authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Estelle Renard (E)

IHU LIRYC, L'Institut des maladies du RYthme Cardiaque, Fondation Bordeaux Université, Bordeaux, France; University of Bordeaux, Inserm, Centre de Recherche Cardio-Thoracique de Bordeaux, Bordeaux, France. Electronic address: estelle.renard@ihu-liryc.fr.

Elodie Surget (E)

IHU LIRYC, L'Institut des maladies du RYthme Cardiaque, Fondation Bordeaux Université, Bordeaux, France; University of Bordeaux, Inserm, Centre de Recherche Cardio-Thoracique de Bordeaux, Bordeaux, France.

Richard D Walton (RD)

IHU LIRYC, L'Institut des maladies du RYthme Cardiaque, Fondation Bordeaux Université, Bordeaux, France; University of Bordeaux, Inserm, Centre de Recherche Cardio-Thoracique de Bordeaux, Bordeaux, France.

Cindy Michel (C)

IHU LIRYC, L'Institut des maladies du RYthme Cardiaque, Fondation Bordeaux Université, Bordeaux, France; University of Bordeaux, Inserm, Centre de Recherche Cardio-Thoracique de Bordeaux, Bordeaux, France.

David Benoist (D)

IHU LIRYC, L'Institut des maladies du RYthme Cardiaque, Fondation Bordeaux Université, Bordeaux, France; University of Bordeaux, Inserm, Centre de Recherche Cardio-Thoracique de Bordeaux, Bordeaux, France.

Virginie Dubes (V)

IHU LIRYC, L'Institut des maladies du RYthme Cardiaque, Fondation Bordeaux Université, Bordeaux, France; University of Bordeaux, Inserm, Centre de Recherche Cardio-Thoracique de Bordeaux, Bordeaux, France.

Bastien Guillot (B)

IHU LIRYC, L'Institut des maladies du RYthme Cardiaque, Fondation Bordeaux Université, Bordeaux, France; University of Bordeaux, Inserm, Centre de Recherche Cardio-Thoracique de Bordeaux, Bordeaux, France.

Marine E Martinez (ME)

IHU LIRYC, L'Institut des maladies du RYthme Cardiaque, Fondation Bordeaux Université, Bordeaux, France; University of Bordeaux, Inserm, Centre de Recherche Cardio-Thoracique de Bordeaux, Bordeaux, France.

Mélèze Hocini (M)

IHU LIRYC, L'Institut des maladies du RYthme Cardiaque, Fondation Bordeaux Université, Bordeaux, France; University of Bordeaux, Inserm, Centre de Recherche Cardio-Thoracique de Bordeaux, Bordeaux, France; CHU de Bordeaux, Département d'électrophysiologie et de stimulation cardiaques, Hôpital Cardiologique du Haut-Lévêque, Pessac, France.

Michel Haïssaguerre (M)

IHU LIRYC, L'Institut des maladies du RYthme Cardiaque, Fondation Bordeaux Université, Bordeaux, France; University of Bordeaux, Inserm, Centre de Recherche Cardio-Thoracique de Bordeaux, Bordeaux, France; CHU de Bordeaux, Département d'électrophysiologie et de stimulation cardiaques, Hôpital Cardiologique du Haut-Lévêque, Pessac, France.

Olivier Bernus (O)

IHU LIRYC, L'Institut des maladies du RYthme Cardiaque, Fondation Bordeaux Université, Bordeaux, France; University of Bordeaux, Inserm, Centre de Recherche Cardio-Thoracique de Bordeaux, Bordeaux, France.

Classifications MeSH